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Down-regulation of plasma intrinsic protein1 aquaporin in poplar trees is detrimental to recovery from embolism.

Identifieur interne : 002279 ( Main/Exploration ); précédent : 002278; suivant : 002280

Down-regulation of plasma intrinsic protein1 aquaporin in poplar trees is detrimental to recovery from embolism.

Auteurs : Francesca Secchi [États-Unis] ; Maciej A. Zwieniecki

Source :

RBID : pubmed:24572173

Descripteurs français

English descriptors

Abstract

During their lifecycles, trees encounter multiple events of water stress that often result in embolism formation and temporal decreases in xylem transport capacity. The restoration of xylem transport capacity requires changes in cell metabolic activity and gene expression. Specifically, in poplar (Populus spp.), the formation of xylem embolisms leads to a clear up-regulation of plasma membrane protein1 (PIP1) aquaporin genes. To determine their role in poplar response to water stress, transgenic Populus tremula × Populus alba plants characterized by the strong down-regulation of multiple isoforms belonging to the PIP1 subfamily were used. Transgenic lines showed that they are more vulnerable to embolism, with 50% percent loss of conductance occurring 0.3 MPa earlier than in wild-type plants, and that they also have a reduced capacity to restore xylem conductance during recovery. Transgenic plants also show symptoms of a reduced capacity to control percent loss of conductance through stomatal conductance in response to drought, because they have a much narrower vulnerability safety margin. Finally, a delay in stomatal conductance recovery during the period of stress relief was observed. The presented results suggest that PIP1 genes are involved in the maintenance of xylem transport system capacity, in the promotion of recovery from stress, and in contribution to a plant's control of stomatal conductance under water stress.

DOI: 10.1104/pp.114.237511
PubMed: 24572173
PubMed Central: PMC3982741


Affiliations:


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Le document en format XML

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<term>Aquaporins (genetics)</term>
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<term>Gene Expression Regulation, Plant (MeSH)</term>
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<term>Aquaporines (métabolisme)</term>
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<term>Arbres (physiologie)</term>
<term>Déshydratation (MeSH)</term>
<term>Facteurs temps (MeSH)</term>
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<term>Populus (génétique)</term>
<term>Populus (physiologie)</term>
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<term>Régulation de l'expression des gènes végétaux (MeSH)</term>
<term>Régulation négative (génétique)</term>
<term>Tiges de plante (physiologie)</term>
<term>Végétaux génétiquement modifiés (MeSH)</term>
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<div type="abstract" xml:lang="en">During their lifecycles, trees encounter multiple events of water stress that often result in embolism formation and temporal decreases in xylem transport capacity. The restoration of xylem transport capacity requires changes in cell metabolic activity and gene expression. Specifically, in poplar (Populus spp.), the formation of xylem embolisms leads to a clear up-regulation of plasma membrane protein1 (PIP1) aquaporin genes. To determine their role in poplar response to water stress, transgenic Populus tremula × Populus alba plants characterized by the strong down-regulation of multiple isoforms belonging to the PIP1 subfamily were used. Transgenic lines showed that they are more vulnerable to embolism, with 50% percent loss of conductance occurring 0.3 MPa earlier than in wild-type plants, and that they also have a reduced capacity to restore xylem conductance during recovery. Transgenic plants also show symptoms of a reduced capacity to control percent loss of conductance through stomatal conductance in response to drought, because they have a much narrower vulnerability safety margin. Finally, a delay in stomatal conductance recovery during the period of stress relief was observed. The presented results suggest that PIP1 genes are involved in the maintenance of xylem transport system capacity, in the promotion of recovery from stress, and in contribution to a plant's control of stomatal conductance under water stress. </div>
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<Citation>Oecologia. 1997 Apr;110(2):191-196</Citation>
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<ArticleId IdType="pubmed">28307424</ArticleId>
</ArticleIdList>
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<Reference>
<Citation>Plant J. 1998 Apr;14(1):121-8</Citation>
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<ArticleId IdType="pubmed">9681029</ArticleId>
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<name sortKey="Secchi, Francesca" sort="Secchi, Francesca" uniqKey="Secchi F" first="Francesca" last="Secchi">Francesca Secchi</name>
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